p53 is the archetypal tumor suppressor, but still a lot remains to be learned about the mechanisms by which p53 exerts its tumor suppressor function. Many target genes have been described, both direct and indirect targets, transcription factors, both protein coding genes and non-coding genes (e.g., miRNAs). However, although it is generally accepted that p53 is a master apoptosis regulator, it is still unknown how p53 makes the switch from arrest/survival to apoptosis. As p53 in some cases even seems to help tumorigenesis, it would be advantageous to identify mechanisms by which p53 stimulates or prevents apoptosis, particularly of cancer cells.
Moreover, since cancer cells have developed an increased ability to survive in sub-optimal environment, even irrespective of the presence or absence of wild-type p53, it would be advantageous to identify targets that can modulate cell survival downstream of p53. Most preferably, such targets would allow selective modulation of the pathway in cancer cells, so that these cells can be selectively killed.